Konishi Masahiro, Nagashima Kei, Kanosue Kazuyuki
Department of Physiology, School of Allied Health Sciences, Osaka University Faculty of Medicine, Yamadaoka 1-7, Suita, Osaka 565-0871, Japan.
J Physiol. 2002 Nov 15;545(1):289-96. doi: 10.1113/jphysiol.2002.027029.
Salt loading decreases body core temperature (T(core)) at neutral ambient temperature (26 degrees C) and increases heat-escape/cold-seeking behaviour in desalivated rats. In this study, we tested the hypothesis that brain angiotensin II (AII) and arginine vasopressin (AVP) are associated with these responses. Surgically desalivated rats (n = 28) were administered an injection (S.C., 10 ml kg(-1)) of either normal saline (154 mM, NS) or hypertonic saline (2500 mM, HS) following an intracerebroventricular injection (10 microl kg(-1)) of an AII AT(1)-receptor antagonist (candesartan, 5 microg microl(-1)), an AVP V(1)-receptor antagonist ((beta-mercapto-beta, beta-cyclopenta-methylene propionyl(1), O-Me-Tyr(2), Arg(8))-vasopressin, 0.5 microg microl(-1)), or normal saline (154 mM). Each rat was placed in a behaviour box, first at 26 degrees C for 1 h to allow the measurement of baseline T(core) and movement. The ambient temperature was then elevated to 40 degrees C for the next 2 h, during which time the rat was able to trigger a 0 degrees C air reward for 30 s by moving into a specific area of the box (operant behaviour). The S.C. HS significantly decreased baseline T(core) at 26 degrees C (36.5 +/- 0.1 degrees C) and increased counts of operant behaviour at 40 degrees C (57 +/- 3) compared with results obtained following S.C. NS injection (37.4 +/- 0.1 degrees C and 42 +/- 1, respectively). These responses to s.c. HS were inhibited by the intracerebroventricular injection of AT(1) (37.3 +/- 0.1 degrees C and 43 +/- 2, respectively; P < 0.05) and V(1) antagonists (37.2 +/- 0.2 degrees C and 42 +/- 2, respectively; P < 0.05), although administration of both antagonists with S.C. NS had no effect. These results suggest that brain AII and AVP are involved in the decrease in T(core) observed at neutral ambient temperature and the increase in heat-escape/cold-seeking behaviour in response to osmotic stimulation, via the central AT(1) and V(1) receptors, respectively
在中性环境温度（26摄氏度）下，盐负荷会降低机体核心温度（T(core)），并增加去唾液腺大鼠的散热/畏寒行为。在本研究中，我们检验了如下假设：脑内血管紧张素II（AII）和精氨酸加压素（AVP）与这些反应相关。对手术去除唾液腺的大鼠（n = 28）进行脑室内注射（10微升/千克）AII AT(1)受体拮抗剂（坎地沙坦，5微克/微升）、AVP V(1)受体拮抗剂（(β-巯基-β,β-环戊亚甲基丙酰(1),O-甲基-Tyr(2),精氨酸(8))-加压素，0.5微克/微升）或生理盐水（154毫摩尔）后，再皮下注射（10毫升/千克）生理盐水（154毫摩尔，NS）或高渗盐水（2500毫摩尔，HS）。将每只大鼠置于行为箱中，首先在26摄氏度下放置1小时以测量基线T(core)和活动情况。然后将环境温度升至40摄氏度，持续2小时，在此期间大鼠若进入箱内特定区域（操作性行为），就能触发30秒的0摄氏度空气奖励。与皮下注射NS后的结果（分别为37.4±0.1摄氏度和42±1）相比，皮下注射HS显著降低了26摄氏度时的基线T(core)（36.5±0.1摄氏度），并增加了40摄氏度时的操作性行为次数（57±3）。脑室内注射AT(1)拮抗剂（分别为37.3±0.1摄氏度和43±2；P<0.05）和V(1)拮抗剂（分别为37.2±0.2摄氏度和42±2；P<0.05）可抑制对皮下注射HS的这些反应，尽管同时给予两种拮抗剂和皮下注射NS没有效果。这些结果表明，脑内AII和AVP分别通过中枢AT(1)和V(1)受体，参与了在中性环境温度下观察到的T(core)降低以及对渗透压刺激的散热/畏寒行为增加。
